Ischemic injury causes tissue remodeling over time. This produces dyssynchronous, hypokinetic, dyskinetic or akinetic tissue function. One mechanism that perpetuates tissue remodeling (termed systolic stretch) occurs when viable ventricular tissue contracts, producing pressure that causes less viable or non-viable tissue to be forced outward. This bulging of the less viable or non-viable tissue dissipates the pumping force of the heart and adversely impacts cardiac output. The heart attempts to compensate for this decrease in cardiac output by increasing contractility and/or heart rate. However, the degree of systolic stretch progressively increases over time, continuing to reduce cardiac output, enlarge the volume of remodeled tissue, and exacerbate the potential for rupture of the affected tissue.
One condition that can result from such remodeling is cardiomyopathy, a typically chronic disorder of heart muscle that may involve hypertrophy and obstructive damage to the heart. A current approach for treating end-stage cardiomyopathy involves resecting a significant portion of the left ventricular free wall to reduce the size of the left ventricular cavity. The procedure, developed by Randas J. V. Batista, attempts to improve the relationship between volume, mass, and diameter. In reducing the volume of the left ventricle, investigators have observed a decrease in mitral regurgitation but a concomitant decrease in diastolic compliance. This decreases diastolic filling, which adversely impacts the complete cardiac cycle.
Other approaches for treating cardiomyopathy include reshaping the heart chambers using tethers, balloons, external bands, or other tension structures to reduce the end-diastolic diameters of the ventricles. PCT Pamphlets WO 98/29041 entitled “Heart Wall Tension Reduction Apparatus and Method”; WO 99/30647 entitled “Valve to Myocardium Tension Members Device and Method”; WO 00/06026 entitled “Heart Wall Tension Reduction Apparatus and Method”; WO 00/06027 entitled “Stress Reduction Apparatus and Method”; WO 00/06028 entitled “Transventricular Implant Tools and Devices”; WO 00/16700 entitled “External Stress Reduction Device and Method” describe tethers or bands that change the geometry of the heart and restrict the maximum outer diameters of the ventricles. The tethers are positioned inside the heart and extend from one side of the ventricle to the other to exert tension on opposite sides of the heart. The bands are positioned around the epicardial surface of the ventricles and restrict expansion of the ventricles. The tethers and bands only limit local wall tension and maximal end-diastolic diameter; they do not directly assist in systolic ejection or diastolic filling of the heart. Nor do they distribute loading over a large region of heart tissue.